Molecular mimicry and autoimmunity

Journal of Autoimmunity, Journal Year: 2018, Volume and Issue: 95, P. 100 - 123

Published: Oct. 26, 2018

Molecular mimicry is one of the leading mechanisms by which infectious or chemical agents may induce autoimmunity. It occurs when similarities between foreign and self-peptides favor an activation autoreactive T B cells a foreign-derived antigen in susceptible individual. However, molecular unlikely to be only underlying mechanism for autoimmune responses; other factors such as breach central tolerance, non-specific bystander activation, persistent antigenic stimuli (amongst others) also contribute development diseases. Host genetics, exposure microbiota environmental chemicals are additional links our understanding mimicry. Our current knowledge detailed limited issues prolonged periods latency before appearance disease, lack enough statistical power epidemiological studies, limitations potential role genetics human relevance inbred murine models diverse population especially technology systematically dissect T-cell repertoire B-cell responses. Nevertheless, studies on T-cells that generated secondary mimicry, diversity receptor repertoires auto-reactive T-cells, cryptic antigens, generation responses, interaction adjuvants with host immune systems all provide clues advancing involved evolving concept potentially aid prevention treatment

Language: Английский

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Reaction of Human Monoclonal Antibodies to SARS-CoV-2 Proteins With Tissue Antigens: Implications for Autoimmune Diseases

Frontiers in Immunology, Journal Year: 2021, Volume and Issue: 11

Published: Jan. 19, 2021

We sought to determine whether immune reactivity occurs between anti-SARS-CoV-2 protein antibodies and human tissue antigens, molecular mimicry COVID-19 viral proteins tissues could be the cause. applied both monoclonal anti-SARS-Cov-2 (spike protein, nucleoprotein) rabbit polyclonal (envelope membrane protein) 55 different antigens. found that SARS-CoV-2 had reactions with 28 out of representing a diversity groups included barrier proteins, gastrointestinal, thyroid neural tissues, more. also did selective epitope mapping using BLAST showed similarities homology spike, nucleoprotein, many other antigens mitochondria M2, F-actin TPO. This extensive cross-reactivity antigen may play role in multi-system disease process COVID-19, influence severity disease, precipitate onset autoimmunity susceptible subgroups, potentially exacerbate subjects have pre-existing autoimmune diseases. Very recently, were approved for use on patients COVID-19. The used this study are almost identical these antibodies. Thus, our results can establish potential risk disorders come from own dreaded virus, thus ensure badly-needed vaccines treatments being developed it truly safe against disease.

Language: Английский

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The Role of Monocytes and Macrophages in Autoimmune Diseases: A Comprehensive Review

Frontiers in Immunology, Journal Year: 2019, Volume and Issue: 10

Published: May 24, 2019

Monocytes (Mo) and macrophages (Mφ) are key components of the innate immune system involved in regulation initiation, development resolution many inflammatory disorders. In addition, these cells also play important immunoregulatory tissue-repairing roles to decrease reactions promote tissue regeneration. Several lines evidence have suggested a causal link between presence or activation autoimmune diseases. Mo Mφ infiltration diseased tissues is hallmark several However, detailed contributions cells, whether they actually initiate disease perpetuate progression, their phenotype functional alteration merely epiphenomena still unclear Additionally, little known about heterogeneous populations different Elucidating relevance diseases associated mechanisms could lead identification more effective therapeutic strategies future.

Language: Английский

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Autoimmunity is a hallmark of post-COVID syndrome

Journal of Translational Medicine, Journal Year: 2022, Volume and Issue: 20(1)

Published: March 16, 2022

Abstract Autoimmunity has emerged as a characteristic of the post-COVID syndrome (PCS), which may be related to sex. In order further investigate relationship between SARS-CoV-2 and autoimmunity in PCS, clinical serological assessment on 100 patients was done. Serum antibody profiles against self-antigens infectious agents were evaluated by an antigen array chip for 116 IgG 104 IgM antibodies. Thirty pre-pandemic healthy individuals included control group. The median age 49 years (IQR: 37.8 55.3). There 47 males. time 219 143 258) days. Latent polyautoimmunity found 83% 62% patients, respectively. Three developed overt autoimmune disease. antibodies IL-2, CD8B, thyroglobulin more than 10% patients. Other autoantibodies, such anti-interferons, positive 5–10% Anti-SARS-CoV-2 > 85% positively correlated with age, body mass index (BMI). Few autoantibodies influenced BMI. no effect gender over- or under-expression autoantibodies. anti-IFN-λ associated persistence respiratory symptoms. summary, is latent correlates humoral response SARS-CoV-2.

Language: Английский

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Antinuclear Antibodies in Systemic Sclerosis: an Update

Clinical Reviews in Allergy & Immunology, Journal Year: 2019, Volume and Issue: 58(1), P. 40 - 51

Published: Jan. 3, 2019

Language: Английский

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A20/Tumor Necrosis Factor α-Induced Protein 3 in Immune Cells Controls Development of Autoinflammation and Autoimmunity: Lessons from Mouse Models

Frontiers in Immunology, Journal Year: 2018, Volume and Issue: 9

Published: Feb. 21, 2018

Immune cell activation is a stringently regulated process, as exaggerated innate and adaptive immune responses can lead to autoinflammatory autoimmune diseases. Autoinflammation autoimmunity are mediated by aberrantly activated cells, either or cells. Perhaps the best-characterized molecular pathway in nuclear factor-κB (NF-κB) signalling leading transcription of numerous pro-inflammatory cell-survival genes. NF-κB tightly controlled several mechanisms, including key regulatory zinc-finger (de)ubiquitinating enzyme A20/TNFAIP3. Single nucleotide polymorphisms (SNPs) vicinity TNFAIP3 gene associated with spectrum chronic systemic inflammatory diseases, indicating its clinical relevance. Mice harboring targeted cell-specific deletions Tnfaip3 cells like macrophages spontaneously develop disease. In contrast, when involved response, dendritic B-cells for A20/TNFAIP3 deletion, mice spontaneous inflammation that resemble human Therefore, more knowledge on function beneficial our understanding autoinflammation autoimmunity. Using above mentioned mouse models, novel functions have recently been described such control necroptosis inflammasome activity. this review, we discuss enzyme, critical role various Lastly, latest findings SNPs diseases address genotyping may guide treatment decisions.

Language: Английский

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Immunometabolism in the development of rheumatoid arthritis

Immunological Reviews, Journal Year: 2020, Volume and Issue: 294(1), P. 177 - 187

Published: Jan. 27, 2020

Abstract In rheumatoid arthritis (RA), breakdown of self‐tolerance and onset clinical disease are separated in time space, supporting a multi‐hit model which emergence autoreactive T cells is pinnacle pathogenic event. Determining factors cell differentiation survival include antigen recognition, but also the metabolic machinery that provides energy biosynthetic molecules for building. Studies patients with RA have yielded disease‐specific signature, enables naive CD4 to differentiate into pro‐inflammatory helper prone invade tissue elicit inflammation through immunogenic death. A typifying property shunting glucose away from glycolytic mitochondrial processing toward pentose phosphate pathway, favoring anabolic over catabolic reactions. Key defects been localized mitochondria lysosome; including instability DNA due lack repair nuclease MRE11A inefficient lysosomal tethering AMPK deficiency N‐myristoyltransferase 1 (NMT1). The molecular taxonomy metabolically reprogrammed includes enzymes (glucose‐6‐phosphate dehydrogenase, phosphofructokinase), (MRE11A, ATM), regulators protein trafficking (NMT1), membrane adapter TSK5. As mechanisms determining abnormal behavior unraveled, opportunities will emerge interject autoimmune by targeting their checkpoints.

Language: Английский

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The challenges of primary biliary cholangitis: What is new and what needs to be done

Journal of Autoimmunity, Journal Year: 2019, Volume and Issue: 105, P. 102328 - 102328

Published: Sept. 20, 2019

Language: Английский

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Autoimmune phenomena following SARS-CoV-2 vaccination

International Immunopharmacology, Journal Year: 2021, Volume and Issue: 99, P. 107970 - 107970

Published: July 10, 2021

Language: Английский

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Microbial Transglutaminase—The Food Additive, a Potential Inducing Factor in Primary Biliary Cholangitis

Molecules, Journal Year: 2025, Volume and Issue: 30(4), P. 762 - 762

Published: Feb. 7, 2025

Microbial transglutaminase (mTG) is a bacterial survival factor, which frequently used as food additive. This results in the formation of immunogenic epitopes that may cause autoimmunity. Primary biliary cholangitis (PBC) cholestatic, autoimmune liver disease characterized by presence characteristic autoantibodies. The aim this work was to determine epitope similarity and cross-reactivity between mTG- PBC-specific antigens investigate whether microbial enzyme be associated with induction autoimmunity due cross-reactivity. Monoclonal polyclonal antibodies against mTG were applied nine different using ELISA technique. They reacted significantly four out antigens. reaction most pronounced for gp210 PML protein. We also performed vitro studies on impact specific antigen-antibody binding sera PBC patients. found share homology sequences. noticed inhibition PDC M2, gp210, PML, KLHL12 mimics major targets human-specific Cross-reactivity indicate link development diseases.

Language: Английский

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